Glucose and mannose analogs inhibit KSHV replication by blocking N-glycosylation and inducing the unfolded protein response.
Mariana SchlesingerChristian McDonaldAnuj AhujaCarolina Alejandra Alvarez CaneteZelmira Nuñez Del PradoJulian NaipauerTheodore LampidisEnrique A MesriPublished in: Journal of medical virology (2022)
Kaposi's sarcoma-associated herpesvirus (KSHV) is the etiological agent for Kaposi's sarcoma (KS), an HIV/AIDS-associated malignancy. Effective treatments against KS remain to be developed. The sugar analog 2-deoxy- d-glucose (2-DG) is an anticancer agent that is well-tolerated and safe in patients and was recently demonstrated to be a potent antiviral, including KSHV and severe acute respiratory syndrome coronavirus 2. Because 2-DG inhibits glycolysis and N-glycosylation, identifying its molecular targets is challenging. Here we compare the antiviral effect of 2-DG with 2-fluoro-deoxy- d-glucose, a glycolysis inhibitor, and 2-deoxy-fluoro- d-mannose (2-DFM), a specific N-glycosylation inhibitor. At doses similar to those clinically achievable with 2-DG, the three drugs impair KSHV replication and virion production in iSLK.219 cells via downregulation of viral structural glycoprotein expression (K8.1 and gB), being 2-DFM the most potent KSHV inhibitor. Consistently with the higher potency of 2-DFM, we found that d-mannose rescues KSHV glycoprotein synthesis and virus production, indicating that inhibition of N-glycosylation is the main antiviral target using d-mannose competition experiments. Suppression of N-glycosylation by the sugar drugs triggers ER stress. It activates the host unfolded protein response (UPR), counteracting KSHV-induced inhibition of the protein kinase R-like endoplasmic reticulum kinase branch, particularly activating transcription factor 4 and C/EBP homologous protein expression. Finally, we demonstrate that sugar analogs induce autophagy (a prosurvival mechanism) and, thus, inhibit viral replication playing a protective role against KSHV-induced cell death, further supporting their direct antiviral effect and potential therapeutic use. Our work identifies inhibition of N-glycosylation leading to ER stress and UPR as an antienveloped virus target and sugar analogs such as 2-DG and the newly identified 2-DFM as antiviral drugs.
Keyphrases
- cell death
- endoplasmic reticulum
- hiv aids
- sars cov
- respiratory syndrome coronavirus
- endoplasmic reticulum stress
- end stage renal disease
- transcription factor
- protein kinase
- drug induced
- induced apoptosis
- chronic kidney disease
- high glucose
- cell cycle arrest
- oxidative stress
- blood glucose
- positron emission tomography
- ejection fraction
- molecular docking
- diabetic rats
- dna damage
- gene expression
- type diabetes
- cell proliferation
- newly diagnosed
- computed tomography
- coronavirus disease
- binding protein
- tyrosine kinase
- dna methylation
- adipose tissue
- antiretroviral therapy
- genome wide
- insulin resistance
- peritoneal dialysis
- anti inflammatory
- blood pressure
- small molecule
- hiv infected
- amino acid
- hepatitis c virus
- single molecule